The human fetus is well-tolerated in utero regardless of its genetic composition, an accommodation the applicant refers to as fetomaternal tolerance (FMT). The induction of FMT is thought to be the result of suppression of potential allogeneic responses in the uterus and decidua. The major immune cell type in the uterus that could mediate rejection is the natural killer (NK) cell, suggesting that this cell type must be tolerized to the developing human in utero. Decidual NK (dNK) cells express morphological characteristics consistent with an activated phenotype but nonetheless are tolerant of fetal cytotrophoblasts. The predominant model for the induction of tolerance suggests that dNK cells do not respond to cytotrophoblasts because they express the restricted polymorphism major histocompatibility antigen designated HLA-G on their surface. The applicant proposes another paradigm, in which glycoconjugate- induced tolerance in the NK cell response is responsible for inducing FMT. In this model, glycoproteins such as embryonic alpha fetoprotein (AFP) and decidual glycodelin-A use their oligosaccharides to bind the carbohydrate recognition domains of specific killer cell activation and inhibition receptors (KARs and KIRs) expressed on the surface of dNK cells. This interaction induces the expression of the activated NK cell phenotype that is highly tolerant to fetal cells expressing the appropriate glycoconjugate signals such as HLA-G. The primary goal of this study is to carry out experiments complementing preliminary studies in support of this glycoconjugate-based model.